946 resultados para lotus embryo


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被子植物成熟的种子一般不合有叶绿素,但是莲(Nelumbo nucifera Gaertn.)的胚芽却具有鲜明的绿色,本文较详细地研究了莲胚芽不同于一般被子植物叶组织的色素和光台系统组成,并通过对莲胚芽成熟发育过程中的叶绿素合成和光合系统发育进行分析,探讨了莲胚芽光合特性形成的原因,最后对莲胚芽在黑暗中萌发能发育并建成光合系统的现象进行了研究,主要的结果如下: 1,莲胚芽不仅含有叶绿素和光合系统,而且其色素和光台系统组成均与莲叶以及其它被子植物的叶组织不同。莲胚芽的Chla/b值约为0.8左右,远远低于正常高等植物的Chla/b值(~3):莲胚芽的色素组成中不含有β-胡萝卜素;莲胚芽的光合系统没有电子传递活性,快速荧光动力学测定结果表明莲胚芽只有较高的固定荧光F。没有可变荧光Fv;原位低温荧光光谱检测表明莲胚芽只在679nm处有一个荧光发射主峰,没有正常的PSII和PSI荧光发射峰(683nm、692nm和730nm);部分变性的叶绿素蛋白复合物凝胶电泳分析结果表明莲胚芽叶绿体类囊体膜上只存在LHCII 一种叶绿素蛋白复合物(其中单体和二聚体形式的LHCII均有发现);Western Blots检测结果表明莲胚芽的LHCII组成比较单一,同时确证了莲胚芽不含有PSI的核心和天线蛋白组分。莲胚芽LHCII和莲叶LHCII在SDS-PAGE图谱上迁移距离相同,但是光谱分析表明二者不仅在Chla、Chlb的相对含量上不同,而且在叶绿素分子与蛋白的结合状态上也存在差异,这些差异主要是由一部分Chla分子造成的,Chlb分子在二者中的结合状态则比较~致。 2,对莲胚芽成熟过程中的光合系统发育进行研究,结果表明这个过程可以分为建成期(0-20天)、稳定期(20-30天)和降解期(30—40天)三个阶段。在建成期和稳定期内,莲胚芽外面的包被物可能不是完全遮光的,所以莲胚芽能感受到环境光信号,其叶绿素合成已经光合系统建成集中在此阶段内进行:在莲’胚芽成熟后期,莲胚芽外面的包被组织开始木质化,光信号无法再穿透它们,莲胚芽的光合系统发育进入降解期,叶绿素合成停止,己建成的光合系统开始降解,到莲胚芽成熟时,除LHCIl外,光合系统其余的叶绿素蛋白复合物都被降解了,所以莲胚芽具有不同于一般祓子植物叶组织的色素和光合系统组成。对莲胚芽的成熟发育过程进行遮光处理,结果发现遮光发育的莲胚芽发生明显黄化,这表明莲胚芽的叶绿素合成也离不开光照,在莲总基因组中检测不到编码DPOR的三个基因的同源序列,确证了莲胚芽不具有在黑暗中合成叶绿素的能力。 3,在黑暗中萌发生长的莲胚芽能够在相当长的时间内保持其叶绿素稳定,特别是Chla的含量在暗生长10天以内基本没有变化;原位低温荧光光谱检测表明暗萌发过程中莲苗有PSII和PSI的荧光发射峰形成,暗生长10天左右的莲苗具有比较明显的光合系统荧光发射峰,但是与自然光照下的发育过程相比,暗萌发莲苗的光合系统荧光发射峰出现较慢,而且PSI的荧光发射相对较弱;暗萌发莲苗在转绿以及冻融过程中的原位低温荧光光谱变化表明莲苗在黑暗中建成的光合系统不完善并且不稳定;对莲胚芽、暗萌发莲苗以及莲叶的叶绿体吸收光谱进行比较,结果显示暗萌发莲苗的叶绿体发育阶段介于莲胚芽和莲叶之间;叶绿素蛋白复合物凝胶电泳分离,SDS-PAGE,Western Blots免疫检测、以及叶绿素荧光诱导动力学结果均确证暗萌发莲苗有光合系统的发育,特别是PSI的出现;对暗萌发莲苗的光化学活性进行分析,结果表明暗中建成的PSII和PSI均具有电子传递活性:但是放氧复合物的发育不完全,对莲胚芽暗萌发过程光合系统建成的原因进行分析,推测叶绿素可能起了至关重要的作用,光对于莲胚芽萌发过程中的光合系统发育来说可能并不是必需的。

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Background Huntingtin, the HD gene encoded protein mutated by polyglutamine expansion in Huntington's disease, is required in extraembryonic tissues for proper gastrulation, implicating its activities in nutrition or patterning of the developing embryo. To test these possibilities, we have used whole mount in situ hybridization to examine embryonic patterning and morphogenesis in homozygous Hdhex4/5 huntingtin deficient embryos. Results In the absence of huntingtin, expression of nutritive genes appears normal but E7.0–7.5 embryos exhibit a unique combination of patterning defects. Notable are a shortened primitive streak, absence of a proper node and diminished production of anterior streak derivatives. Reduced Wnt3a, Tbx6 and Dll1 expression signify decreased paraxial mesoderm and reduced Otx2 expression and lack of headfolds denote a failure of head development. In addition, genes initially broadly expressed are not properly restricted to the posterior, as evidenced by the ectopic expression of Nodal, Fgf8 and Gsc in the epiblast and T (Brachyury) and Evx1 in proximal mesoderm derivatives. Despite impaired posterior restriction and anterior streak deficits, overall anterior/posterior polarity is established. A single primitive streak forms and marker expression shows that the anterior epiblast and anterior visceral endoderm (AVE) are specified. Conclusion Huntingtin is essential in the early patterning of the embryo for formation of the anterior region of the primitive streak, and for down-regulation of a subset of dynamic growth and transcription factor genes. These findings provide fundamental starting points for identifying the novel cellular and molecular activities of huntingtin in the extraembryonic tissues that govern normal anterior streak development. This knowledge may prove to be important for understanding the mechanism by which the dominant polyglutamine expansion in huntingtin determines the loss of neurons in Huntington's disease.

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“There it went!—Our last little bit of capital, our going back to civilization money . . .” So Charmian Clift fretted when she watched her husband George Johnson hand over a large number of drachma notes to buy a house on the Greek Island of Hydra in 1956. Whereas today’s expatriates fly back and forth between home and away with ease, Clift’s commitment to Hydra meant that a return to Australia, “to civilization”, would always be difficult and perhaps impossible...

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Involving the biopsy of an eight-cell embryo, PGD has been hailed as a means of making reproductive decisions without having to face the heart-wrenching decision to abort an affected foetus. However, controversy around the kinds of traits for which testing can be done, and who has access to the technology, has led to questions about the way in which the technology is developing. Women who are allowed to access in vitro fertilisation (IVF) services can currently also access PGD in limited circumstances.

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The development of the new reproductive technologies has presented significant challenges for policy makers and law reformers. This article focuses on the particular challenges posed by cryopreservation of embryos. These issues are analysed through discussion of relevant Australian statutory provisions and United States case law. The article concludes with a consideration of whether the property model provides an appropriate framework for reproductive material.

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Recent arguments on the ethics of stem cell research have taken a novel approach to the question of the moral status of the embryo. One influential argument focuses on a property that the embryo is said to posses—namely, the property of being an entity with a rational nature or, less controversially, an entity that has the potential to acquire a rational nature—and claims that this property is also possessed by a somatic cell. Since nobody seriously thinks that we have a duty to preserve the countless such cells we wash off our body every day in the shower, the argument is intended as a reductio ad absurdum of the claim that the embryo should be afforded the same moral status as a fully developed human being. This article argues that this argument is not successful and that it consequently plays into the hands of those who oppose embryonic stem cell research. It is therefore better to abandon this argument and focus instead on the different argument that potentiality, as such, is not a sufficient ground for the creation of moral obligations towards the embryo.

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This project assessed the efficiency of lotus reducing the amount of nutrients that are generated in a freshwater aquaculture system. Barramundi were produced at a stocking density similar to industry practices. Lotus was grown to determine if it was capable at reducing the nutrient loading from an aquaculture system

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. The changes in the net amounts of retinol, retinyl esters and retinal in both the developing chick embryo and the newly hatched chick were investigated. The embryo requires about 68nmol of the vitamin for its growth, whereas the baby chick requires about 108nmol during the first 7 days after hatching. 2. Retinal was present in the egg in fairly high concentrations at the beginning of the incubation but it virtually disappeared from the extra-embryonic tissue after day 17 of incubation. It was not found in the liver of the embryo or of the newly hatched chick up until day 7.

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Chick embryo tRNA, prepared by a simple large-scale method, was fractionated on three different ion-exchange columns. In all cases simple chromatographic patterns for various tRNA species were observed, indicating the presence of only a few major species of tRNA for each amino acid. By repeated chromatography one species of alanine tRNA was purified to approx. 80% purity. T1 ribonuclease digest of this purified tRNA gave a simple chromatographic pattern. Because of the simplicity of the method of preparation of tRNA from this readily available source and the presence of only a few species of tRNA for each amino acid, chick embryo is suited for the study of tRNA and its various functions in higher systems.

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A simple method for preparing bulk quantities of tRNA from chick embryo has been developed. In this method chick embryos were homogenized in a buffer of pH 4.5, followed by deproteinization with phenol. The aqueous layer was allowed to separate under gravity. The resulting aqueous layer, after two more phenol treatments, was directly passed through a DEAE-cellulose column and the tRNA eluted therefrom with 1 Image NaCl. The tRNA prepared by this method was as active as the one prepared at neutral pH.

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The in vitro development of hamster preimplantation embryos is supported by non-glucose energy substrates. To investigate the importance of embryonic metabolism, influence of succinate and malate on the development of hamster 8-cell embryos to blastocysts was examined using a chemically defined protein-free modified hamster embryo culture medium-2 (HECM-2m). There was a dose-dependent influence of succinate on blastocyst development; 0.5 mM succinate was optimal (85.1% ± 3.9 vs. 54.5% ± 3.5). In succinate-supplemented HECM-2m, blastocyst development was reduced by omission of lactate (68.5% ± 7.2), but not pyruvate (85.8% ± 6.2) or glutamine (84.1% ± 2.1). Succinate along with either glutamine or lactate or pyruvate poorly supported blastocyst development (28%-58%). Malate also stimulated blastocyst development; 0.01 mM malate was optimal (86.3% ± 2.8). Supplementation of both succinate and malate to HECM-2m supported maximal (100%) blastocyst development, which was inhibited 4-fold by the addition of glucose/phosphate. The mean cell numbers (MCN) of blastocysts cultured in succinate-supplemented HECM-2m was higher (28.3 ± 1.1) than it was for those cultured in the absence of glutamine or pyruvate (range 20-24). The MCN was the highest (33.4 ± 1.6) for blastocysts cultured in succinate-malate-supplemented HECM-2m followed by those in succinate (28.3 ± 1.1) or malate (24.7 ± 0.5) supplemented HECM-2m. Embryo transfer experiments showed that 29.8% (±4.5) of transferred blastocysts cultured in succinate-malate-supplemented HECM-2m produced live births, similar (P > 0.1) to the control transfers of freshly recovered 8-cells (33.5% ± 2.0) or blastocysts (28.9% ± 3.0). These data show that supplementation of succinate and malate to HECM-2m supports 100% development of hamster 8-cell embryos to high quality viable blastocysts and that non-glucose oxidizable energy substrates are the most preferred components in hamster embryo culture medium. Mol. Reprod. Dev. 47:440-447, 1997. © 1997 Wiley-Liss, Inc.